ArticleNeurotoxicology and teratology
The Notch target E(spl)mδ is a muscle-specific gene involved in methylmercury toxicity in motor neuron development.
Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Review: myogenic and muscle toxicity targets of environmental methylmercury exposure.Archives of toxicology · 2024Review
- Notch Signaling in Insect Development: A Simple Pathway with Diverse Functions.International journal of molecular sciences · 2023Review
- Perspectives on the Drosophila melanogaster Model for Advances in Toxicological Science.Current protocols · 2023Review
- Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Tissue-specific Nrf2 signaling protects against methylmercury toxicity in Drosophila neuromuscular development.Archives of toxicology · 2020Article
- Article
- Post-Developmental Roles of Notch Signaling in the Nervous System.Biomolecules · 2020Review
- Methylmercury modifies temporally expressed myogenic regulatory factors to inhibit myoblast differentiation.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- Drosophotoxicology: Elucidating Kinetic and Dynamic Pathways of Methylmercury Toxicity in a Drosophila Model.Frontiers in genetics · 2019Article
- Methylmercury and diphenyl diselenide interactions in Drosophila melanogaster: effects on development, behavior, and Hg levels.Environmental science and pollution research international · 2018Article
- Methylmercury exposure causes a persistent inhibition of myogenin expression and C2C12 myoblast differentiation.Toxicology · 2018Article
- Notch Target Gene E(spl)mδ Is a Mediator of Methylmercury-Induced Myotoxicity inFrontiers in genetics · 2017Article
- Article
- Methylmercury exposure during early Xenopus laevis development affects cell proliferation and death but not neural progenitor specification.Neurotoxicology and teratologyArticle
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Methylmercury (MeHg) is a ubiquitous environmental toxin that has a selective and potent impact on the nervous system, particularly during neural development yet, the mechanisms for its apparent neurodevelopmental specificity are unknown. The Notch receptor pathway has been implicated as a MeHg target in several studies. Notch signaling mediates cell-cell signals in a number of developmental contexts including neurogenesis and myogenesis, where it fundamentally acts to repress differentiation. Previous work in our lab has shown that MeHg causes preferential upregulation of a canonical Notch response gene, E(spl)mδ, in Drosophila embryos. In parallel, MeHg is seen to disrupt outgrowth of embryonic intersegmental motor nerves (ISN), which can be mimicked by expression of activated Notch in embryonic neurons. However, overexpression of E(spl)mδ in developing neurons fails to elicit motor neuron outgrowth defects, pointing to a non-autonomous role for E(spl)mδ in motor axon development. In this study we investigate a role for E(spl)mδ in conveying the toxicity of MeHg in the embryo. We find that endogenous expression of the E(spl)mδ gene localizes to developing somatic muscles in embryos. Notably, E(spl)mδ expression is seen in several muscles that are known synaptic targets for both the ISN and the segmental motor nerve (SN). We also demonstrate that the SN, similar to the ISN, exhibits disrupted axon outgrowth in response to MeHg. E(spl)mδ can induce a SN motor neuron phenotype, similar to MeHg treatment; but, only when E(spl)mδ expression is targeted to developing muscles. E(spl)mδ overexpression in developing muscles also results in aberrant muscle morphology, which is not apparent with expression of the closely related E(spl)mγ in developing muscles. Our data point to a role for the Notch target E(spl)mδ in mediating MeHg toxicity in embryonic development by disrupting the coordinated targeting of motor neurons to their muscle targets.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.